In prostate cancer, where androgen deprivation causes prostate carcinoma and stromal cells to upregulate the IGFBP5 level (75, 76), overexpression of IGFBP5 enhances the anti-apoptotic and mitogenic activity of recombinant IGF1 protein, thereby helping to overcome castration-induced tumor regression (77, 78). This evidence concerns the gene IGFBP5 and prostate carcinoma.